Roles of Small RNAs in Virus-Plant Interactions

Abstract

Small RNAs (sRNAs), including microRNAs (miRNAs) and short interfering RNAs (siRNAs), are non-coding but powerful RNA molecules of 20-30 nucleotides in length. sRNAs play crucial regulatory roles in diverse plant biological processes. Recently, many studies on sRNAs have been reported. We summarize new findings of sRNAs in virus-plant interactions to accelerate the function analysis of sRNAs. The main content of this review article includes three parts: virus-responsive sRNAs, function analysis of sRNAs in virus pathogenicity or host resistance, and some sRNAs-mediated underlying mechanisms in virus-plant interactions. New findings of sRNAs deepen our understanding about sRNAs' roles, which might contribute to the design of novel control measures against plant viruses.

Keywords: microRNAs; resistance; short interfering RNAs; small RNAs; symptom induction.

Figure 1

The schematic diagram of biogenesis and action modes of small RNAs (sRNAs). MIR are transcripted by RNA polymerase II producing pri-miRNAs with hairpin structure. Mature miRNAs are produced by processing complex including Dicer-like RNase III (DCL), Hyponastic leaves/Double strand RNA binding protein (HYL/DRB), Serrate (SE), and Hua enhancer (HEN) proteins. Mature miRNA is incorporated into action mode complex to direct the target silencing by cleavage or methylation. Based on the difference in origin, siRNAs are divided into endogenous or exogenous siRNAs. Viral genome or replication intermediates all can form hairpin structure. Additionally, host native or viral siRNA-directed double strand RNAs are the origin of sRNAs’ biogenesis. Double strand RNAs are processed by processing complex, which mainly include DCL, Argonaut (AGO), Suppressor of genesilencing (SGS), and RDR (RNA-dependent RNA polymerase) proteins to produce siRNAs. Mature siRNA is incorporated into action mode complex to direct the target silencing by cleavage or methylation at transcriptional or post transcriptional level.

Figure 2

sRNAs-mediated viral pathogenic and resistant mechanisms. Left column of the figure is resistant mechanisms (A–D), right column of the figure is susceptible mechanisms (E–G). (A) Cotton leaf curl Burewala virus (CLCuBV) induces the expression of miR168. The miRNA can directly target virus genome, enhancing viral resistance. (B) Rice stripe virus (RSV) induces the accumulation of miR444. MADS23/27a/57 are targets of miR444, and they can bind to the promoter of RDR1 (RNA-dependent RNA polymerase), inhibiting the expression of RDR1. So, miR444 indirectly triggered RDR1-mediated viral resistance. (C) Plant hormone JA mediated viral resistance. Responsive to rice ragged stunt virus (RRSV) infection, miR319 is induced and negatively regulates TCP21, and further suppresses JA-mediated viral resistance. (D) In rice, AGO18 functions as a miRNA locker, competitively binding to miR168 or miR528 to increase AGO1- or ROS-mediated viral resistance. (E) CMV Y-Sat prompts the production of siRNAs by inducing the expression of AGO1. These siRNAs direct the cleavage of Chll (chlorophyll biosynthetic gene) mRNA. Tobacco Chll is responsible for the chlorophyll biogenesis, so, the plant displayed viral disease symptoms. (F) RSV infection suppresses the accumulation level of miR171b, which targets OsSCL6-IIabc to accelerate the accumulation of virus. (G) In tobacco, 21-nt nta-miR6020, which is derived from 22-nt miR3019, targets R protein, suppressing domain resistance.